[Chloroquine- and chlorphentermin-induced lipidosis in rat retina] Effects of prenatal co-administration of phentermine and dexfenfluramine in rats. Use of dexfenfluramine, fenfluramine and phentermine and the risk of stroke. Ionamin online references

Ionamin online research references

Klin Monatsbl Augenheilkd. 1999 Mar;214(3):178-82.
[Chloroquine- and chlorphentermin-induced lipidosis in rat retina]

[Article in German]

Bredehorn T, Duncker GI.

Klinik und Poliklinik fur Augenheilkunde der Martin-Luther-Universitat Halle-Wittenberg.

BACKGROUND: The amphiphilic drugs chloroquine and chlorphentermine are known to cause lipidosis in the human and rat retina. METHODS: We treated femal albino Wistar rats orally with chloroquine for 12 weeks, followed by a period of 4 months with normal feed and another group with chlorphentermine for 4-16 weeks. The animals were submitted to electroretinography, and the retinae were prepared for histological investigations. RESULTS: Chloroquine caused severe lipidosis in the neuroretina and slight photoreceptor cell degeneration after 12 weeks of treatment. The b-wave was reduced to 30% of initial values. After withdrawal the lipidosis remitted, but the degeneration of the photoreceptor cell layer continued to progress. The a-wave and b-wave amplitudes were reduced to 25% and 16% of initial values, respectively. Chlorphentermine caused pronounced lipidosis in the pigment epithelium and less numerous in the neuroretina after 16 weeks; no photoreceptor cell degeneration was found. The b-wave was reduced to 80% of initial values, the a-wave appeared unaffected. CONCLUSION: Whether lipidosis is the primary cause of changes in the electroretinogram and of receptor cell degeneration is doubtful. Excessive lipid storage may be the cause of secondary changes. It is unlikely that lipidosis in pigment epithelium played a role.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10220731&dopt=Abstract

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Eur J Pharmacol. 1999 Mar 26;369(3):R1-3.
Effects of prenatal co-administration of phentermine and dexfenfluramine in rats.

Bratter J, Gessner IH, Rowland NE.

Department of Psychology, University of Florida, Gainesville 32611-2250, USA.

Pregnant rats were infused with phentermine plus dexfenfluramine from days 3 through 17 of gestation. Control rats were either pair-fed or were fed ad libitum. There were no effects of prenatal drug treatment on number of offspring, their birth weights, or on their motor coordination assessed at 11 days of age. Mothers and pups were sacrificed 21 days postpartum. Drug-treated mothers, but not their pups, showed a reduced density of serotonergic axons in the hippocampus compared with controls. 25% of the pups from the prenatal drug group showed mitral valve thickening.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10225380&dopt=Abstract

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Br J Clin Pharmacol. 1999 May;47(5):565-9.
Use of dexfenfluramine, fenfluramine and phentermine and the risk of stroke.

Derby LE, Myers MW, Jick H.

The Boston Collaborative Drug Surveillance Program, Boston University Medical Center, 11 Muzzey Street, Lexington, MA 02173, USA.

AIMS: To estimate the incidence of newly diagnosed idiopathic stroke among users of fenfluramine, dexfenfluramine and phentermine compared to obese nonusers. METHODS: We conducted a cohort study with nested case-control analysis utilizing data from the General Practice Research Database in the UK. Eight thousand four hundred and twenty-three subjects aged 69 years or less at the start of follow-up were exposed to at least one of the three study drugs and 17 225 similarly obese subjects were not exposed to any of the study drugs. RESULTS: We identified 45 incident cases of idiopathic CVA in this cohort of subjects. The incidence of CVA among all current users of a diet drug was 1.3/1000 person-years (95% CI 0.5, 3.5). The incidence for current fenfluramine users (n=2) was 2.6/1000 person-years (95% CI 0.7, 9.6), for current dexfenfluramine users (n=1) 1.1/1000 person-years (95% CI 0.3, 3.8), and for current phentermine users 0/1000 person-years (95% CI 0.0, 12.9). The incidence in obese nonusers was 0.6/1000 person-years (95% CI 0.4, 0. 9). The adjusted matched odds ratio (OR) for thrombotic stroke from the case-control analysis comparing current use of a diet drug to nonuse was 2.4 (95% CI 0.6, 9.1). There was only one exposed subject among seven who had haemorrhagic stroke. CONCLUSIONS: The incidence of CVA in generally young obese subjects during use of fenfluramine, dexfenfluramine or phentermine is low. Although we found an OR of 2. 4 comparing users of any of the anorexiants with nonusers, this is based on only three exposed cases and the confidence limits are wide. We conclude that our study does not support a substantial increased risk of stroke attributable to the use of fenfluramine, dexfenfluramine or phentermine.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10336582&dopt=Abstract

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